scholarly journals Long non-coding RNAs in regulation of adipogenesis and adipose tissue function

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Tiziana Squillaro ◽  
Gianfranco Peluso ◽  
Umberto Galderisi ◽  
Giovanni Di Bernardo
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Drug Targets ◽  
Metabolic Diseases ◽  
Tissue Development ◽  
Cellular Functions ◽  
Adipose Tissue Development ◽  
And Function

Complex interaction between genetics, epigenetics, environment, and nutrition affect the physiological activities of adipose tissues and their dysfunctions, which lead to several metabolic diseases including obesity or type 2 diabetes. Here, adipogenesis appears to be a process characterized by an intricate network that involves many transcription factors and long noncoding RNAs (lncRNAs) that regulate gene expression. LncRNAs are being investigated to determine their contribution to adipose tissue development and function. LncRNAs possess multiple cellular functions, and they regulate chromatin remodeling, along with transcriptional and post-transcriptional events; in this way, they affect gene expression. New investigations have demonstrated the pivotal role of these molecules in modulating white and brown/beige adipogenic tissue development and activity. This review aims to provide an update on the role of lncRNAs in adipogenesis and adipose tissue function to promote identification of new drug targets for treating obesity and related metabolic diseases.

scholarly journals Undernutrition and stage of gestation influence fetal adipose tissue gene expression

2015 ◽  
Vol 54 (3) ◽  
pp. 263-275 ◽  
Author(s):  
Jacqueline M Wallace ◽  
John S Milne ◽  
Raymond P Aitken ◽  
Dale A Redmer ◽  
Lawrence P Reynolds ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Fatty Acid Synthase ◽  
Uncoupling Protein ◽  
Tissue Development ◽  
Maternal Undernutrition ◽  
Pat Gene ◽  
Adipose Tissue Development ◽  
And Function ◽  
The Impact

Low birthweight is a risk factor for neonatal mortality and adverse metabolic health, both of which are associated with inadequate prenatal adipose tissue development. In the present study, we investigated the impact of maternal undernutrition on the expression of genes that regulate fetal perirenal adipose tissue (PAT) development and function at gestation days 89 and 130 (term=145 days). Singleton fetuses were taken from adolescent ewes that were either fed control (C) intake to maintain adiposity throughout pregnancy or were undernourished (UN) to maintain conception weight but deplete maternal reserves (n=7/group). Fetal weight was independent of maternal intake at day 89, but by day 130, fetuses from UN dams were 17% lighter and had lower PAT mass that contained fewer unilocular adipocytes. Relative PAT expression ofIGF1,IGF2,IGF2Rand peroxisome proliferator-activated receptor gamma (PPARG) mRNA was lower in UN than in controls, predominantly at day 89. Independent of maternal nutrition, PAT gene expression ofPPARG, glycerol-3-phosphate dehydrogenase, hormone sensitive lipase, leptin, uncoupling protein 1 and prolactin receptor increased, whereasIGF1,IGF2,IGF1RandIGF2Rdecreased between days 89 and 130. Fatty acid synthase and lipoprotein lipase (LPL) mRNAs were not influenced by nutrition or stage of pregnancy. Females had greaterLPLand leptin mRNA than males, andLPL, leptin andPPARGmRNAs were decreased in UN at day 89 in females only. PAT gene expression correlations with PAT mass were stronger at day 89 than they were at day 130. These data suggest that the key genes that regulate adipose tissue development and function are active beginning in mid-gestation, at which point they are sensitive to maternal undernutrition: this leads to reduced fetal adiposity by late pregnancy.

scholarly journals Long Noncoding RNAs: Novel Important Players in Adipocyte Lipid Metabolism and Derivative Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Bin Zhang ◽  
Saijun Xu ◽  
Jinyan Liu ◽  
Yong Xie ◽  
Sun Xiaobo
Keyword(s):  
Adipose Tissue ◽  
Drug Targets ◽  
Metabolic Diseases ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Public Health Issue ◽  
Global Public Health ◽  
Tissue Development ◽  
Adipose Tissue Development ◽  
Excessive Adiposity

Obesity, a global public health issue, is characterized by excessive adiposity and is strongly related to some chronic diseases including cardiovascular diseases and diabetes. Extra energy intake-induced adipogenesis involves various transcription factors and long noncoding RNAs (lncRNAs) that control lipogenic mRNA expression. Currently, lncRNAs draw much attention for their contribution to adipogenesis and adipose tissue function. Increasing evidence also manifests the pivotal role of lncRNAs in modulating white, brown, and beige adipose tissue development and affecting the progression of the diseases induced by adipose dysfunction. The aim of this review is to summarize the roles of lncRNAs in adipose tissue development and obesity-caused diseases to provide novel drug targets for the treatment of obesity and metabolic diseases.

scholarly journals Vitamin D signalling in adipose tissue

2012 ◽  
Vol 108 (11) ◽  
pp. 1915-1923 ◽  
Author(s):  
Cherlyn Ding ◽  
Dan Gao ◽  
John Wilding ◽  
Paul Trayhurn ◽  
Chen Bing
Keyword(s):  
Vitamin D ◽  
Adipose Tissue ◽  
Vitamin D Deficiency ◽  
Vitamin D Metabolites ◽  
Hydroxyvitamin D ◽  
The Metabolic Syndrome ◽  
Prevalence Of Obesity ◽  
Adipose Tissue Development ◽  
And Function

Vitamin D deficiency and the rapid increase in the prevalence of obesity are both considered important public health issues. The classical role of vitamin D is in Ca homoeostasis and bone metabolism. Growing evidence suggests that the vitamin D system has a range of physiological functions, with vitamin D deficiency contributing to the pathogenesis of several major diseases, including obesity and the metabolic syndrome. Clinical studies have shown that obese individuals tend to have a low vitamin D status, which may link to the dysregulation of white adipose tissue. Recent studies suggest that adipose tissue may be a direct target of vitamin D. The expression of both the vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes has been shown in murine and human adipocytes. There is evidence that vitamin D affects body fat mass by inhibiting adipogenic transcription factors and lipid accumulation during adipocyte differentiation. Some recent studies demonstrate that vitamin D metabolites also influence adipokine production and the inflammatory response in adipose tissue. Therefore, vitamin D deficiency may compromise the normal metabolic functioning of adipose tissue. Given the importance of the tissue in energy balance, lipid metabolism and inflammation in obesity, understanding the mechanisms of vitamin D action in adipocytes may have a significant impact on the maintenance of metabolic health. In the present review, we focus on the signalling role of vitamin D in adipocytes, particularly the potential mechanisms through which vitamin D may influence adipose tissue development and function.

scholarly journals Enhanced nutritionally induced adipose tissue development in mice with stromelysin-1 gene inactivation

2003 ◽  
Vol 89 (04) ◽  
pp. 696-704 ◽  
Author(s):  
Erik Maquoi ◽  
Diego Demeulemeester ◽  
Gabor Vörös ◽  
Désire Collen ◽  
H. Lijnen
Keyword(s):  
Adipose Tissue ◽  
Research Society ◽  
The Body ◽  
Tissue Development ◽  
Cholesterol Levels ◽  
Fat Deposits ◽  
Adipose Tissue Development ◽  
Adipocyte Hypertrophy ◽  
Deficient Mice

SummaryTo investigate a potential role of stromelysin-1 (MMP-3) in development of adipose tissue, 5 week old male MMP-3 deficient mice (MMP-3-/-) and wild-type (MMP-3+/+) controls were kept on a high fat diet (HFD) for 15 weeks. MMP-3-/- mice were hyperphagic and gained more weight than the MMP-3+/+ mice. At the time of sacrifice, the body weight of the MMP-3-/- mice was significantly higher than that of the MMP-3+/+ mice, as was the weight of the isolated subcutaneous (SC) and gonadal (GON) fat deposits. Significant adipocyte hypertrophy was observed in the GON but not in the SC adipose tissue of MMP-3-/- mice. Fasting plasma glucose and cholesterol levels were comparable in both genotypes, whereas triglyceride levels were significantly lower in MMP-3-/- mice. Staining with an endothelial cell specific lectin revealed a significantly higher blood vessel density and larger total stained area in the GON adipose tissues of MMP-3-/- mice. Thus, in a murine model of nutritionally induced obesity, MMP-3 impairs adipose tissue development, possibly by affecting food intake and/or adipose tissue-related angiogenesis.Theme paper: Part of this paper was originally presented at the joint meetings of the 16th International Congress of the International Society of Fibrinolysis and Proteolysis (ISFP) and the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September, 2002.

Influence of t-PA and u-PA on Adipose Tissue Development in a Murine Model of Diet-Induced Obesity

2002 ◽  
Vol 87 (02) ◽  
pp. 306-310 ◽  
Author(s):  
P.E. Morange ◽  
D. Bastelica ◽  
M.F. Bonzi ◽  
B. Van Hoef ◽  
D. Collen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator ◽  
The Body ◽  
Tissue Type ◽  
Tissue Development ◽  
Diet Induced Obesity ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Adipose Tissue Development

SummaryTo investigate the potential role of tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA) in development of adipose tissue, we have used a nutritionally induced obesity model in t-PA (t-PA−/−) and u-PA (u-PA−/−) deficient mice. Five week old male wild-type (WT), t-PA−/− or u-PA−/− mice (n = 9 to 16) were fed a high fat diet (HFD, 42% fat). After 16 weeks of HFD, the body weight of t-PA−/− mice was significantly higher than that of WT mice (48 ± 1.1 g vs. 39 ± 2.2 g, p = 0.004). The total weight of the isolated subcutaneous (sc) fat deposit was higher in t-PA−/− than in WT mice (2.4 ± 0.22 g vs. 1.2 ± 0.29 g, p = 0.002), accompanied with higher adipocyte diameters (80 ± 1.7 µm vs. 61 ± 4.7 µm, p < 0.01). These differences were not observed in the intra-abdominal fat deposit. The number of stroma cells in both adipose tissue territories was increased in t-PA−/− as compared to WT mice (2.0 ± 0.13 vs. 1.5 ± 0.10 p = 0.02 and 3.0 ± 0.17 vs 1.6 ± 0.17, p = 0.0001, stroma cells/ adipocytes in sc and intra-abdominal tissue, respectively), partly as a result of an increased number of endothelial cells (192 ± 9 vs. 154 ± 18 p = 0.06 and 108 ± 13 vs. 69 ± 8 p = 0.04 CD31 stained/adipocyte area). In contrast the weight gain and adipose tissue development in u-PA−/− mice was not different from that in WT mice. These data suggest that t-PA but not u-PA plays a role in adipose tissue development.

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